Infants born with fetal alcohol syndrome often suffer from an increased incidence of illness due to immunodeficiency at both the humoral and cell- mediated levels. Recent work from this lab suggests that exposure to ethanol in utero causes a delay in B cell development in the fetal liver, then in the spleen and bone marrow of neonatal animals. Our working hypothesis is that a delay in the development of B lineage cells in the fetal liver would account for the diminished number of B cells in the spleen and bone marrow of neonatal mice exposed to ethanol in utero. The goals of this proposal are to determine the effects of in utero ethanol exposure has on: 1) The appearance of lymphoid precursors, in the fetal liver, which can commit to the B cell lineage. 2) The number of B cell developmental intermediates in the fetal liver at various time points during gestation. 3) The functional ability and expansion of B cell developmental intermediates in the fetal liver.